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Cell Growth & Differentiation, Vol 1, Issue 9 401-406, Copyright © 1990 by American Association of Cancer Research
ARTICLES |
RJ Leach, AN Magewu, JD Buckley, WF Benedict, C Rother, AL Murphree, S Griegel, MF Rajewsky and PA Jones
Kenneth Norris Jr. Comprehensive Cancer Center, University of Southern California, Los Angeles 90033.
The origins of the initial mutations in sporadic retinoblastoma were explored using polymorphic markers from chromosome 13q. The paternal chromosome was maintained in 3 of 3 informative bilateral tumors which had undergone reduction to homozygosity for regions of this chromosome. The paternal chromosome was maintained in 7 of 8 informative unilateral tumors which likewise demonstrated a reduction of homozygosity. These data are in contrast to previously published studies of chromosome retention in unilateral retinoblastoma [Dryja, T. P., Mukai, S., Petersen, R., Rapaport, J. M., Walton, D., and Yandel, D. W. Nature (Lond.), 339: 556-558, 1989; Zhu, Z., Dunn, J. M., Phillips, R. A., Goddard, A. D., Paton, K. E., Becker, A., and Gallie, B. L. Nature (Lond.), 340: 312-313, 1989] and provide the first evidence that genomic imprinting may play a role in this disease.
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| Cancer Research | Clinical Cancer Research |
| Cancer Epidemiology Biomarkers & Prevention | Molecular Cancer Therapeutics |
| Molecular Cancer Research | Cell Growth & Differentiation |